Host factors which govern the various phases of herpes keratitis may now be studied much more definitively in the mouse because of 2 new developments: (1) the establishment of an ocular mouse model, and (2) the possibility of applying selective immunosuppression using new and highly specific deletion techniques to suppress antibody production, T cell-dependent immunity, and interferon production, respectively. Specifically (1) anti-micron chain antibody specifically suppresses antibody production leaving intact cell-mediated immunity and interferon responses. (2) Anti-theta serum suppresses cell-mediated immunity, helper function and T dependent humoral responses without affecting the interferon system. (3) Anti-interferon serum suppresses interferon action. We propose to apply these techniques to a newly established murine herpes keratitis model to explore the defensive mechanisms which govern recovery of the eye lesions, viral latency in the central nervous system, and recurrences. Appropriate reconstitution experiments will be planned as indicated by the outcome of the deletion experiments.